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10.1136/annrheumdis-2013-204900 http://scihub22266oqcxt.onion/10.1136/annrheumdis-2013-204900 C4428954!4428954!24914072     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Ann+Rheum+Dis 2015 ; 74 (11): 2062-9 Nephropedia Template TP {{tp|p=24914072|t=2015. Gadolinium-based Compounds Induce NLRP3-dependent IL-1? Production and Peritoneal Inflammation |pdf=|usr=}}{{24914072}} gab.com Text Gadolinium-based Compounds Induce NLRP3-dependent IL-1 Production and Peritoneal Inflammation JO: Ann Rheum Dis http://www.kidney.de/pget.php?&tw=1&pmid=24914072 #FOAvip Objective: Nephrogenic systemic fibrosis (NSF) is a progressive fibrosing disorder that may develop in patients with chronic kidney disease (CKD) after administration of gadolinium-based contrast agents (GBCAs). In the setting of impaired renal clearance of GBCAs, gadolinium (Gd) deposits in various tissues and fibrosis subsequently develops. However, the precise mechanism by which fibrosis occurs in NSF is incompletely understood. Because other profibrotic agents, such silica or asbestos, activate the NOD-like receptor protein 3 (NLRP3) inflammasome and initiate IL-1? release with the subsequent development of fibrosis, we evaluated the effects of GBCAs on inflammasome activation. Methods: Bone marrow derived macrophages (BMDM) from C57BL/6, Nlrp3?/? and Asc?/? mice were incubated with three Gd-containing compounds and IL-1? activation and secretion was detected by ELISA and Western blot analysis. Inflammasome activation and regulation was investigated in IL-4- and IFN?-polarized macrophages by ELISA, qRT-PCR and NanoString nCounter analysis. Furthermore, C57BL/6 and Nlrp3?/? mice were injected i.p. with GBCA and recruitment of inflammatory cells to the peritoneum was analyzed by FACS. Results: Both free Gd and GBCAs activate the NLRP3 inflammasome and induce IL-1? secretion in vitro. Gd-DTPA also induces the recruitment of neutrophils and inflammatory monocytes to the peritoneum in vivo. Gd activated IL-4-polarized macrophages more effectively than IFN?-polarized macrophages, which preferentially expressed genes known to downregulate inflammasome activity. Conclusion: These data suggest that Gd released from GBCAs triggers a NLRP3 inflammasome-dependent inflammatory response that leads to fibrosis in an appropriate clinical setting. The preferential activation of IL-4-differentiated macrophages is consistent with the predominantly fibrotic presentation of NSF. Twit Text FOAVip Gadolinium-based Compounds Induce NLRP3-dependent IL-1 Production and Peritoneal Inflammation ????Ann Rheum Dis http://www.kidney.de/pget.php?&tw=1&pmid=24914072 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24914072 #FOAvip English Wikipedia <ref>{{Cite pmid|24914072}}</ref> Gadolinium-based Compounds Induce NLRP3-dependent IL-1? Production and Peritoneal Inflammation #MMPMID24914072 Schmidt-Lauber C; Bossaller L; Abujudeh HH; Vladimer GI; Christ A; Fitzgerald KA; Latz E; Gravallese EM; Marshak-Rothstein A; Kay J Ann Rheum Dis 2015[Nov]; 74 (11): 2062-9 PMID24914072show ga Objective: Nephrogenic systemic fibrosis (NSF) is a progressive fibrosing disorder that may develop in patients with chronic kidney disease (CKD) after administration of gadolinium-based contrast agents (GBCAs). In the setting of impaired renal clearance of GBCAs, gadolinium (Gd) deposits in various tissues and fibrosis subsequently develops. However, the precise mechanism by which fibrosis occurs in NSF is incompletely understood. Because other profibrotic agents, such silica or asbestos, activate the NOD-like receptor protein 3 (NLRP3) inflammasome and initiate IL-1? release with the subsequent development of fibrosis, we evaluated the effects of GBCAs on inflammasome activation. Methods: Bone marrow derived macrophages (BMDM) from C57BL/6, Nlrp3?/? and Asc?/? mice were incubated with three Gd-containing compounds and IL-1? activation and secretion was detected by ELISA and Western blot analysis. Inflammasome activation and regulation was investigated in IL-4- and IFN?-polarized macrophages by ELISA, qRT-PCR and NanoString nCounter analysis. Furthermore, C57BL/6 and Nlrp3?/? mice were injected i.p. with GBCA and recruitment of inflammatory cells to the peritoneum was analyzed by FACS. Results: Both free Gd and GBCAs activate the NLRP3 inflammasome and induce IL-1? secretion in vitro. Gd-DTPA also induces the recruitment of neutrophils and inflammatory monocytes to the peritoneum in vivo. Gd activated IL-4-polarized macrophages more effectively than IFN?-polarized macrophages, which preferentially expressed genes known to downregulate inflammasome activity. Conclusion: These data suggest that Gd released from GBCAs triggers a NLRP3 inflammasome-dependent inflammatory response that leads to fibrosis in an appropriate clinical setting. The preferential activation of IL-4-differentiated macrophages is consistent with the predominantly fibrotic presentation of NSF. äGadolinium-based Compounds Induce NLRP3-dependent IL-1? Production and(epmc).pdf DeepDyve Pubget Overpricing